Scientists at Jefferson Medical College and Mount Sinai School of Medicine have identified a protein that plays a leading part in triggering kidney disease in diabetic patients, a condition known as diabetic nephropathy and the leading cause of kidney failure worldwide. The finding, which they report February 22 in the journal PLoS Medicine, could lead to the eventual development of compounds that might be used to treat diabetic kidney disease. According to study co-author Kumar Sharma, M.D., director of the Center for Diabetic Kidney Disease at Thomas Jefferson University in Philadelphia and professor of medicine at Jefferson Medical College of Thomas Jefferson University, more than 40 percent of patients with end-stage chronic kidney disease also have diabetic nephropathy. While diabetic nephropathy affects approximately one in three people with type 1 and type 2 diabetes, how diabetes damages the kidneys is poorly understood.
Dr. Sharma, along with Erwin Böttinger, M.D., professor of medicine and pharmacology and biological chemistry at Mount Sinai School of Medicine in New York, and their co-workers looked at kidney samples from mice and people with and without diabetes and looked at the effects of high glucose on the kidney cells.
The researchers found that a protein called CD36 was present in a specific cell type called the proximal tubular epithelial cell in human diabetic kidney disease. In humans, the cells seem to be involved in a self-directed cell death or apoptosis in diabetic kidney disease.